Guillain-Barre syndrome pathology

Pathological conditions in which capsaicin itself is not sufficiently active, but more potent vanilloids are expected to be of greater therapeutic value. For example diabetic neuropathy (Ross and Varipapa, 1989), postherpetic neuralgia (Watson et al., 1988 Bernstein et al., 1989), chronic distal painful polyneuropathy (Low et al., 1995), post-mastectomy pain syndrome (Watson et al., 1989), Guillain-Barre syndrome (Morgenlander et al., 1990), reflex sympathetic dystrophy (Cheshire and Snyder, 1990), vulvar vestibulitis (Friedrich, 1988). 

Griffin JW, Li CY, Ho TW, Tian M, Gao CY, Xue P, Mishu B, Comb-lath DR, Macko C, McKhann GM, Asbury AK (1996a) Pathology of the motor-sensory axonal Guillain-Barre Syndrome. Ann Neurol 39 17-28. 

Prineas JW (1981) Pathology of the Guillain-Barre syndrome. Ann Neurol 9(Suppl) 6-19. 

Sheikh KA, Ramos-Alvarez M, Jackson AC, Li CY, Asbury AK, Griffin JW (2005) Overlap of pathology in paralytic rabies and axonal Guillain-Barre syndrome. Ann Neurol 57 768-772. 

GSLs, because they are shed into the CSF, may be potential markers for brain pathology. In addition, shed GSLs or bacterial GSL structural mimics may also act as antigens in peripheral neuropathies like Guillain-Barre syndrome and multifocal motor neuropathy. 

Following observations of the critical role of MMP-9 in animal models resembling multiple sclerosis and Guillain-Barre s syndrome, MMPs have been implicated in several different types of neurologic diseases (C9, R4, V2). Treatment with synthetic inhibitors of MMPs has reversed some of the pathology in animal models of brain injury (R4). TIMPs and MMPs have also been implicated in Alzheimer s disease (P3). 

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